Cardiac Anatomy and Physiology Flashcards
What are the determinants of myocardial oxygen demand?
Wall tension and contractility
How can myocardial oxygen demand be reduced?
1- Decrease intraventricular pressure
2- Prevent or promptly treat ventricular distention
3- decrease heart rate
4- decrease contractility
What is Laplace’s Law?
Laplace’s law states that wall tension is proportional to pressure (P) and chamber radius (r) and inversely proportional to wall thickness (h), as represented
by the equation:
Wall tension = (intracavitary pressure) * (ventricular radius) / (2* wall thickness)
This law is applicable to myocardial wall tension. Increased wall tension results in increased myocardial oxygen consumption.
Patients with chronic hypertension (which imposes an increased pressure load on the left ventricle) commonly have left ventricular hypertrophy (ie, increased thickness of the left ventricular wall). The increased wall thickness (increased h in the above equation) results in a decreased wall tension.
In contrast, patients with decompensated systolic heart failure tend to have dilated cardiomyopathy. The increase in ventricular chamber size (increased r) and thin myocardium (decreased h) results in an increase in wall tension. Treatment of congestive heart failure with diuresis or venodilation reduces preload, resulting in a decreased radius, decreased wall tension, and less myocardial oxygen consumption.
How do you meet myocardial oxygen requirements?
Raise coronary blood flow
The principal mechanism for matching oxygen supply to alterations in myocardial oxygen demand is exquisite regulation and control of coronary blood flow.
What critical factors modify coronary blood flow?
1- Perfusion pressure and vascular tone of the coronary circulation
2- time available for perfusion (determined mainly by heart rate)
3- severity of intraluminal obstructions
4- presence of any collateral circulation
Which area of the heart is most vulnerable to ischemia?
The subendocardium of the left ventricle, which is exposed to LV intracavitary pressure and where metabolic requirements are increased because of greater systolic shortening.
When does perfusion of the left and right subendocardium take place?
Left subendocardium: almost entirely during diastole.
Right subendocardium: diastole and systole, assuming pulmonary hypertension is not present.
What determines the LV coronary perfusion pressure?
The gradient between the aortic diastolic pressure and LV diastolic pressure. In the presence of intraluminal obstruction or increased vascular tone, this pressure gradient is reduced. a low LVDP is ideal for improving perfusion (causes higher pressure gradient) and reducing myocardial oxygen demand. On the other hand, increasing perfusion pressure by raising the aortic pressure will also increase myocardial oxygen demand, but this is less important when one considers that tachycardia is the most important cause of intraoperative and perioperative ischemia.
What is coronary vascular reserve?
the difference between autoregulated, baseline flow, and blood flow available under conditions of maximal vasodilation is termed coronary vascular reserve and is normally 3-5x higher than basal flow. As epicardial coronary stenosis becomes more pronounced, progressive vasodilation of resistance vessels allows preservation of basal flow, but at the cost of reduced reserve.
True or False: It is not uncommon for an anesthetized patient to show signs of ischemia without any changes in heart rate, blood pressure, or ventricular filling pressures.
True: in fact, most ischemic episodes are not accompanied by hemodynamic changes.
True or false: anesthetic decisions should be designed to reduce and control factors that increase myocardial oxygen demand (heart rate, contractility, and wall tension).
True
What are normal PA catheter values for the following:
CVP RA RV PA PCWP
CVP = RVEDP = 3-8 mmHg RA= 0-8 mmHg RV = 15-30 / 0-8 mmHg PA = 15-30 / 3-12 mmHg PCWP = 1-10 mmHg
What are normal left-sided heart values?
LA = 1-10 mmHg LV = 100-140 / 3-12 mmHg Aortic = 100-140 / 60-90 mmHg
Describe the CVP waveform. Specifically, what do the a, c, and v waves represent? What is the x-descent and what is the y-descent?
Waveform Component Phase of Cardiac Cycle Mechanical Event
a wave End diastole Atrial contraction
c wave Early systole Tricuspid bulging (IVC)
v wave Late systole Systolic filling of the atrium
x descent Mid systole Atrial relaxation
y descent Early diastole Early ventricular filling
What is a normal PR interval? What can cause an increase in a PR interval? What can shorten the PR interval?
The PR interval includes the P wave as well as the PR segment. It is measured from the beginning of the P wave to the first part of the QRS complex.
Normal time: 0.12-0.2 sec
The PR interval is shorter at faster heart rates due to sympathetically mediated enhancement of AV nodal conduction; it is longer when the rate is slowed as a consequence of slower AV nodal conduction resulting from withdrawal of sympathetic tone or an increase in vagal inputs. Long PR intervals are usually seen in first degree AV block, but there may be other causes
What is the QRS complex? What is the duration of a normal QRS complex?
The QRS complex represents the time for ventricular depolarization.
The entire QRS duration normally lasts for 0.06 to 0.10 seconds (1½ to 2½ small boxes) and is not influenced by heart rate
What is the length of a normal QT interval? What can prolong a QT interval?
The QT interval consists of the QRS complex, the ST segment, and T wave. Thus, the QT interval is primarily a measure of ventricular repolarization. The time for ventricular repolarization and therefore the QT (or JT) interval is dependent upon the heart rate; it is shorter at faster heart rates and longer when the rate is slower. Thus, a QT interval that is corrected for heart rate (QTc).
The normal value for the QTc in men is ≤0.44 sec and in women is ≤0.45 to 0.46 sec
Bundle branch block can increase the QT interval.
EKG paper and length of the tics:
1- one full box
2- the tiny tics
Each 1 mm (small) horizontal box corresponds to 0.04 second (40 ms), with heavier lines forming larger boxes that include five small boxes and hence represent 0.20 sec (200 ms) intervals
How do you approach EKG interpretation?
Step 1- Calculate the rate.
Step 2: Rhythm — Are P waves present? Is there a P wave before every QRS complex and a QRS complex after every P wave? Are the P waves and QRS complexes regular? Is the PR interval constant?
Step 3: Axis — Is there left or right axis deviation?
Step 4: Intervals — What is the PR interval? Short PR intervals are suggestive of WPW syndrome. Long PR intervals are usually seen in first degree AV block, but there may be other causes. What is the QRS interval? Long QRS intervals represent a bundle branch block, ventricular preexcitation, ventricular pacing, or ventricular tachycardia. What is the QT interval? Short and long QT intervals may be present.
Step 5: P wave — What is the shape and axis of the P wave? The P wave morphology should be examined to determine if the rhythm is sinus or from another atrial location
Step 6: QRScomplex — Is the QRS wide? If so, examination of the morphology can determine if there is left or right bundle branch block or pre-excitation present. In addition, increased voltage may indicate left or right ventricular hypertrophy. Are Q waves present, suggestive of infarction?
Step 7: ST segment-T wave — Is there ST elevation or depression? Are the T waves inverted?
Describe 1st degree AV block.
Prolonged PR interval (> 0.2 seconds), usually clinically insignificant
Describe 2nd degree AV block, Mobitz Type 1.
P-wave normal , PR interval progressively lengthens with each cycle until QRS complex is dropped. PR interval following dropped beat is shorter than normal. Commonly seen in trained athletes.
Describe 2nd degree AV block, Mobitz Type 2.
P waves normal, but some are not followed by QRS complex. In contrast to Mobitz type 1, the PR and RR intervals are constant and the dropped QRS occurs without warning.
